Atkins’ 1972 Diet Revolution was based on 10 years of clinical success!

In April 2003, walking to work at age 72, Dr. Robert Atkins slipped on an icy New York sidewalk, cracked the back of his head open, developed a blood clot – slipped into a coma and died several days later. His untimely death came just as some members of the Medical Establishment were finally beginning to acknowledge that Atkins had been right all along.

Back in 1972, after trying a “high natural fat” diet on himself and thousands of his own patients for 10 years, Atkins wrote Diet Revolution and sold 1 million copies in six months. Immediately vilified by the AMA as a greedy “Fat Doctor,” Atkins had to defend himself and his “high fat” diet before a congressional committee.

Dr. Atkins survived and prospered. As a family doctor and cardiologist, Atkins enjoyed decades of successful clinical experience reversing obesity, diabetes, and heart disease. His thousands of patients over three decades were losing pounds, burning fat, and eating juicy steak – not waiting around for Ancel Keys’ gang to admit they were wrong!

Also, Atkins had no time for mealy-mouthed journalists – baiting them, as it were, with “bacon cheeseburger talk.” And Atkins never claimed to have invented a diet; he learned about “high fat” in the Journal of the American Medical Association’s story about Dr. Alfred Pennington’s success prescribing a high fat diet to overweight, obese DuPont executives.

proof Atkins was right…

Lipoproteins (such as LDL) are lipid-protein emulsion-like particles made up of varying percentages of protein, fat in phospholipid form, and cholesterol. The various lipoproteins transport fat-soluble lipids – such as Vitamin D – in the aqueous blood. (Remember, fat and water don’t mix.)

Lipoproteins are needed to deliver:

Fat – in triglyceride form – Tri-3 fatty acids attached to glycerol

Cholesterol – free and esterified (attached to something)

Fat soluble nutrients such as beta carotene

There are two distinct lipoprotein systems – one for dietary fat and one for liver-made fat. In humans, the chylomicron delivers dietary fat, assembled within the intestinal wall to transport exogenous lipids out to the body.

The chylomicron’s key identifying protein is apolipoprotein B48. ApoB48 is the exclusive marker for fat and other lipids arriving from the diet. ApoB48 wraps around the particle – providing structure and signal identification to cell receptors throughout the body.

Lipoprotein Protein Identifier Function

Chylomicron

apoB48

made in gut – transport dietary lipids

VLDL

apoB100

made in liver – transports liver-made fat

LDL

apoB100

metabolic offspring of VLDL – transports cholesterol

HDL

apoA1

made in liver – reverse cholesterol transport

The second largest lipoprotein is VLDL – very low density lipoprotein – made in the liver to transport liver-made fat (triglycerides). Chylomicrons and VLDL are the triglyceride-rich lipoproteins. If the chylomicron is an 18-wheeler, VLDL’s are smaller UPS-like delivery trucks. Their common duty is to carry fat and other lipids away from the intestines and the liver, respectively.

Triglyceride (three fatty acids attached to glycerol) describes how fat is assembled for delivery in the body, as shown below. The word triglyceride has another meaning in your blood work or lipid profile: Triglyceride (TG) represents how much liver-made fat (triglycerides) is circulating in your blood after fasting 10-12 hours.

Triglyceride: three fatty acids attached to glycerol

The Dietary Fat Pathway

Between meals, the intestines secrete lipid poor chylomicrons, but when fat is absorbed after a meal, the chylomicrons increase in size quickly; great flux in the dietary fat pathway. As they mature into large “B48s,” chylomicrons are dispatched into the blood stream via the lymph.

Chylomicrons have a short half life – 13 to 14 minutes. After a fat-rich meal, say three eggs fried in butter or lard, apoB48s will disappear from the circulation in 2 or 3 hours. Hungry cells spot the B48 marker and quickly snatch up the dietary fat! In your fasting blood work, chylomicrons – B48s – will be too few to measure.

(Chylomicrons can also offload their triglycerides to other lipoproteins. As we will learn in future editions of Diet Heart News, lipoproteins are not discreet particles; they can interact with each other in complex ways. The body wastes nothing!)

The body-made fat pathway

In the circulation, liver-made VLDL – apoB100 – has a very different fate. After about 80 percent of VLDL’s liver-made and liver-assembled triglycerides are off-loaded, VLDL morphs into low density lipoprotein (LDL) – a smaller particle (van) now delivering mostly cholesterol. (There is a short-lived intermediate density lipoprotein – IDL – that is on the spectrum between VLDL and LDL.)

Eat a lot of carbohydrates, especially the easily-digested variety, and your liver will make a lot of fat (Triglyceride) and need plenty of trucks (VLDL) to haul it away:

VLDL – made in the liver to haul away triglycerides made in the liver.

Triglycerides (TG) – in blood work, a measure of residual liver-made fats in the blood.

So there you have it – Atkins was right – carbohydrates – not fats – determine the atherogenicity of the fat and cholesterol traveling in your blood. According to lipid biochemist Michael Gurr, B48 is vastly outnumbered in artery plaque by B100:

“There is some evidence for the presence of apoB48 in arterial lesions, although this is difficult to demonstrate since apoB48 is enormously outnumbered in the circulation by apoB100 (italics mine).”

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